Deaths of two hospital inpatients poisoned by pilocarpine.

Cordner, Stephen; Fysh, R.R.; Gordon, Harvey; Whitaker, S.

doi:10.1136/bmj.293.6557.1285

Cited by 9 publications

(3 citation statements)

References 1 publication

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“…The small dose was used to balance the relief of her moderate symptoms with the risk of anticholinergic side effects including dry mouth. More severe symptoms may be seen in a larger overdose and would most likely require higher doses of atropine (30,31).…”

Section: Discussionmentioning

confidence: 98%

“…All three patients developed confusion and pulmonary edema and two required intravenous atropine (3 mg and 4.8 mg, respectively). Both patients who required atropine died several days later from pneumonia after recovery from the initial cholinergic crisis (31). Systemic muscarinic symptoms have also resulted from leakage of an implanted ophthalmic pilocarpine delivery system (32).…”

Section: Discussionmentioning

confidence: 98%

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Pilocarpine toxicity and the treatment of xerostomia

Hendrickson

Morocco

Greenberg

2004

The Journal of Emergency Medicine

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Pilocarpine toxicity and the treatment of xerostomia

Hendrickson

Morocco

Greenberg

2004

The Journal of Emergency Medicine

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“…The mutant receptors are more sensitive to acetylcholine than normal receptors, and may generate seizures by promoting and synchronizing spontaneous oscillations in thalamo-cortical circuits [ 22 ]. Further, pilocarpine (an acetylcholine muscarinic receptor agonist) is a well described proconvulsant agent [ 23 ] and the blockade of endogenous brain AChEs by organophosphate pesticides or poisons can also cause seizures [ 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

Taenia larvae possess distinct acetylcholinesterase profiles with implications for host cholinergic signalling

Lange

Prodjinotho²,

Tomes

et al. 2020

PLoS Negl Trop Dis

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Larvae of the cestodes Taenia solium and Taenia crassiceps infect the central nervous system of humans. Taenia solium larvae in the brain cause neurocysticercosis, the leading cause of adult-acquired epilepsy worldwide. Relatively little is understood about how cestode-derived products modulate host neural and immune signalling. Acetylcholinesterases, a class of enzyme that breaks down acetylcholine, are produced by a host of parasitic worms to aid their survival in the host. Acetylcholine is an important signalling molecule in both the human nervous and immune systems, with powerful modulatory effects on the excitability of cortical networks. Therefore, it is important to establish whether cestode derived acetylcholinesterases may alter host neuronal cholinergic signalling. Here we make use of multiple techniques to profile acetylcholinesterase activity in different extracts of both Taenia crassiceps and Taenia solium larvae. We find that the larvae of both species contain substantial acetylcholinesterase activity. However, acetylcholinesterase activity is lower in Taenia solium as compared to Taenia crassiceps larvae. Further, whilst we observed acetylcholinesterase activity in all fractions of Taenia crassiceps larvae, including on the membrane surface and in the excreted/secreted extracts, we could not identify acetylcholinesterases on the membrane surface or in the excreted/secreted extracts of Taenia solium larvae. Bioinformatic analysis revealed conservation of the functional protein domains in the Taenia solium acetylcholinesterases, when compared to the homologous human sequence. Finally, using whole-cell patch clamp recordings in rat hippocampal brain slice cultures, we demonstrate that Taenia larval derived acetylcholinesterases can break down acetylcholine at a concentration which induces changes in neuronal signalling. Together, these findings highlight the possibility that Taenia larval acetylcholinesterases can interfere with cholinergic signalling in the host, potentially contributing to pathogenesis in neurocysticercosis.

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A Review of Organophosphate Poisoning

1988

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Many organophosphate compounds are pesticides widely used for the control of insect vectors. They are not ideal agents because they lack target vector selectivity, and have caused severe toxicity and even death in humans and domestic animals. Their toxicity has been recognised since the 1930s, when they were also developed for use as chemical warfare agents. The mechanism of action of organophosphates has been determined in some depth; the understanding of the toxic effects resulting from the inhibition of cholinesterase activity, causing accumulation of acetylcholine at nerve endings has played a major part in providing a rationale for specific antidote treatment using atropine and oximes. However, the most suitable oxime for reactivation of cholinesterases has still not been established with certainty, although pralidoxime is widely recommended. Chronic toxicity, particularly the neuropathic effects, merits further study because it contributes substantially to the long term morbidity in cases of severe acute, or chronic, exposure. Prevention of potentially toxic organophosphate exposure, particularly amongst employees in industries manufacturing or using the compounds and in the most susceptible groups of the population, such as the young and the elderly, should be sought wherever possible. Government authorities should be encouraged to control organophosphate product licensing, manufacture, storage, import, methods of use and delivery, food contamination and disposal.

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Deaths of two hospital inpatients poisoned by pilocarpine.

Cited by 9 publications

References 1 publication

Pilocarpine toxicity and the treatment of xerostomia

Pilocarpine toxicity and the treatment of xerostomia

Taenia larvae possess distinct acetylcholinesterase profiles with implications for host cholinergic signalling

A Review of Organophosphate Poisoning

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